Here, I explored how immune checkpoint blockade (ICB) alters adaptive immunity in renal cell carcinoma by comparing gene expression and immune cell composition across treatment and response groups. Using single-cell RNA sequencing of tumor-infiltrating lymphoid cells, I analyzed how hallmark pathways and immune profiles differ between tumors that received ICB and those that did not, as well as across patients with partial, stable, or progressive responses. ICB-treated tumors showed greater activity in cell proliferation and interferon response pathways, while untreated tumors were enriched for inflammatory and angiogenic signals linked to unchecked tumor growth.
Beyond gene expression, I investigated how ICB reshaped the composition of adaptive immune cells. Tumors with partial responses had significantly higher proportions of 41BB-Lo CD8+ T cells (an exhausted T cell subset associated with long-term immunotherapy response) compared to progressive or untreated cases. Stable response tumors more closely resembled untreated ones, suggesting an incomplete immune activation. These differences showed how both transcriptional programs and immune cell abundance can distinguish effective from ineffective ICB responses, offering insight into the dynamics of adaptive immunity in RCC.